Table 1: Common RA-associated microbes.
Microbes Clinical association Animal study Arthritogenic mechanism
Porphyromonas Clinical association between RA and periodontitis [6-10].
Presence of P. gingivalisDNA in RA patients [17].
Immune responses to P. gingivalisin RA patients [34,35].
Increased anti-P. gingivalisantibodies in subjects with high risk of RA [36].
Immunization with P. gingivalisor P. gingivalisenolase induced or exacerbated arthritis [47-49].
P. gingivalis
facilitated destructive arthritis in CIA mice dependent on its peptidylarginine deiminase [51].
Neo-antigen generation [62].
Molecular mimicry [69].
Bystander activation [47,49].
Direct joint damage [88].
Proteus Clinical association between RA and urinary tract infection [11].
Immune responses to P. mirabilis in RA patients [30-33].
  Molecular mimicry [33].
EBV Clinical association between RA and EBV infection [24].
Presence of EBV DNA and protein in RA patients [21,22].
Immune responses to EBV in RA patients [37,41-43]
EBV induced arthritis in humanized mice [55,56]. Molecular mimicry [70,89].
Superantigen [43,82,83].
Mycoplasma Presence of DNA [18,19] and glycoglycerophospholipids (GGPL) [29] in RA patients.
Immune responses to mycoplasma in RA patients [39,40].
Immunization with mycoplasma arthritidis induced or exacerbated arthritis [46,50,84]. Superantigen [40,50].
Bystander activation [29].